New STEMI guidelines

Primary percutaneous coronary intervention or fibrinolysis for STEMI? What if you don’t have PCI at your hospital?

The new 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction is out and you can get the summary here.

Here’s what they say about initial reperfusion therapy:

Onset of Myocardial Infarction: Recommendations
Regional Systems of STEMI Care, Reperfusion Therapy, and Time-to-Treatment Goals

Class I

1. All communities should create and maintain a regional system of STEMI care that includes assessment and continuous quality improvement of emergency medical services and hospital-based activities. Performance can be facilitated by participating in programs such as Mission: Lifeline and the Door-to-Balloon Alliance.(Level of Evidence: B)

2. Performance of a 12-lead electrocardiogram (ECG) by emergency medical services personnel at the site of first medical contact (FMC) is recommended in patients with symptoms consistent with STEMI.(Level of Evidence: B)

3. Reperfusion therapy should be administered to all eligible patients with STEMI with symptom onset within the prior 12 hours. (Level of Evidence: A)

4. Primary PCI is the recommended method of reper- fusion when it can be performed in a timely fashion by experienced operators. (Level of Evidence: A)

5. Emergency medical services transport directly to a PCI-capable hospital for primary PCI is the recommended triage strategy for patients with STEMI, with an ideal FMC-to-device time system goal of 90 minutes or less.(Level of Evidence: B)

6. Immediate transfer to a PCI-capable hospital for primary PCI is the recommended triage strategy for patients with STEMI who initially arrive at or are transported to a non–PCI-capable hospital, with an FMC-to-device time system goal of 120 minutes or less.(Level of Evidence: B)

7. In the absence of contraindications, fibrinolytic therapy should be administered to patients with STEMI at non–PCI-capable hospitals when the anticipated FMC-to-device time at a PCI-capable hospital exceeds 120 minutes because of unavoidable delays.(Level of Evidence: B)

8. When fibrinolytic therapy is indicated or chosen as the primary reperfusion strategy, it should be administered within 30 minutes of hospital arrival.(Level of Evidence: B)

Class IIa

1. Reperfusion therapy is reasonable for patients with STEMI and symptom onset within the prior 12 to 24 hours who have clinical and/or ECG evidence of ongoing ischemia. Primary PCI is the preferred strategy in this population. (Level of Evidence: B)

2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction: Executive Summary: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.
Circulation. 2012 Dec 17. [Epub ahead of print]

Potassium levels and AMI death

An association is demonstrated between abnormal (both high and low) serum potassium levels and in-hospital mortality in patients with acute myocardial infarction. These findings do not necessarily imply a causal relationship, since abnormal potassium levels might be a marker of increased risk of death due to other illness factors rather than a risk of death per se.

Acknowledging that a randomised trial of potassium replacement is unlikely to happen, the authors pragmatically advise:

Our data suggest that the optimal range of serum potassium levels in AMI patients may be between 3.5 and 4.5 mEq/L and that potassium levels of greater than 4.5 mEq/L are associated with increased mortality and should probably be avoided.

Context Clinical practice guidelines recommend maintaining serum potassium levels between 4.0 and 5.0 mEq/L in patients with acute myocardial infarction (AMI). These guidelines are based on small studies that associated low potassium levels with ventricular arrhythmias in the pre−β-blocker and prereperfusion era. Current studies examining the relationship between potassium levels and mortality in AMI patients are lacking.

Objective To determine the relationship between serum potassium levels and in-hospital mortality in AMI patients in the era of β-blocker and reperfusion therapy.

Design, Setting, and Patients Retrospective cohort study using the Cerner Health Facts database, which included 38 689 patients with biomarker-confirmed AMI, admitted to 67 US hospitals between January 1, 2000, and December 31, 2008. All patients had in-hospital serum potassium measurements and were categorized by mean postadmission serum potassium level (<3.0, 3.0-<3.5, 3.5-<4.0, 4.0-<4.5, 4.5-<5.0, 5.0-<5.5, and ≥5.5 mEq/L). Hierarchical logistic regression was used to determine the association between potassium levels and outcomes after adjusting for patient- and hospital-level factors.

Main Outcome Measures All-cause in-hospital mortality and the composite of ventricular fibrillation or cardiac arrest.

Results There was a U-shaped relationship between mean postadmission serum potassium level and in-hospital mortality that persisted after multivariable adjustment. Compared with the reference group of 3.5 to less than 4.0 mEq/L (mortality rate, 4.8%; 95% CI, 4.4%-5.2%), mortality was comparable for mean postadmission potassium of 4.0 to less than 4.5 mEq/L (5.0%; 95% CI, 4.7%-5.3%), multivariable-adjusted odds ratio (OR), 1.19 (95% CI, 1.04-1.36). Mortality was twice as great for potassium of 4.5 to less than 5.0 mEq/L (10.0%; 95% CI, 9.1%-10.9%; multivariable-adjusted OR, 1.99; 95% CI, 1.68-2.36), and even greater for higher potassium strata. Similarly, mortality rates were higher for potassium levels of less than 3.5 mEq/L. In contrast, rates of ventricular fibrillation or cardiac arrest were higher only among patients with potassium levels of less than 3.0 mEq/L and at levels of 5.0 mEq/L or greater.

Conclusion Among inpatients with AMI, the lowest mortality was observed in those with postadmission serum potassium levels between 3.5 and <4.5 mEq/L compared with those who had higher or lower potassium levels.

Serum Potassium Levels and Mortality in Acute Myocardial Infarction
JAMA Jan 11 2012,307(2):115-213

AMI mortality increased as the number of risk factors declined

An interesting finding: in patients with myocardial infarction, hospital mortality increased consistently as the number of risk factors declined. There was also an inverse relationship between age and the number of coronary heart disease risk factors.

The authors discuss the possibility that the some of the zero risk factor group may have had risk factors unknown to the patient or not reported in the history, or may have had other factors that influence the disease, for example insulin resistance, abdominal obesity, psychosocial factors, poor nutrition, or physical inactivity.

Context Few studies have examined the association between the number of coronary heart disease risk factors and outcomes of acute myocardial infarction in community practice.

Objective To determine the association between the number of coronary heart disease risk factors in patients with first myocardial infarction and hospital mortality.

Design Observational study from the National Registry of Myocardial Infarction, 1994-2006.

Patients We examined the presence and absence of 5 major traditional coronary heart disease risk factors (hypertension, smoking, dyslipidemia, diabetes, and family history of coronary heart disease) and hospital mortality among 542 008 patients with first myocardial infarction and without prior cardiovascular disease.

Main Outcome Measure All-cause in-hospital mortality.

Results A majority (85.6%) of patients who presented with initial myocardial infarction had at least 1 of the 5 coronary heart disease risk factors, and 14.4% had none of the 5 risk factors. Age varied inversely with the number of coronary heart disease risk factors, from a mean age of 71.5 years with 0 risk factors to 56.7 years with 5 risk factors (P for trend < .001). The total number of in-hospital deaths for all causes was 50 788. Unadjusted in-hospital mortality rates were 14.9%, 10.9%, 7.9%, 5.3%, 4.2%, and 3.6% for patients with 0, 1, 2, 3, 4, and 5 risk factors, respectively. After adjusting for age and other clinical factors, there was an inverse association between the number of coronary heart disease risk factors and hospital mortality adjusted odds ratio (1.54; 95% CI, 1.23-1.94) among individuals with 0 vs 5 risk factors. This association was consistent among several age strata and important patient subgroups.

Conclusion Among patients with incident acute myocardial infarction without prior cardiovascular disease, in-hospital mortality was inversely related to the number of coronary heart disease risk factors.

Number of Coronary Heart Disease Risk Factors and Mortality in Patients With First Myocardial Infarction
JAMA. 2011;306(19):2158-2159

Supplemental oxygen decreases LV perfusion in volunteers

Oxygen therapy in normoxic acute coronary syndrome patients is controversial, and a previous systematic review cautioned against it in uncomplicated MI. A volunteer study using cardiac imaging demonstrates the effects of supplemental oxygen on coronary blood flow.

 

OBJECTIVES: Oxygen (O2) is a cornerstone in the treatment of critically ill patients, and the guidelines prescribe 10-15 l of O2/min even to those who are initially normoxic. Studies using indirect or invasive methods suggest, however, that supplemental O2 may have negative cardiovascular effects. The aim of this study was to test the hypothesis, using noninvasive cardiac magnetic resonance imaging, that inhaled supplemental O2 decreases cardiac output (CO) and coronary blood flow in healthy individuals.

METHODS: Sixteen healthy individuals inhaled O2 at 1, 8 and 15 l/min through a standard reservoir bag mask. A 1.5 T magnetic resonance imaging scanner was used to measure stroke volume, CO and coronary sinus blood flow. Left ventricular (LV) perfusion was calculated as coronary sinus blood flow/LV mass.

RESULTS: The O2 response was dose-dependent. At 15 l of O2/min, blood partial pressure of O2 increased from an average 11.7 to 51.0 kPa with no significant changes in blood partial pressure of CO2 or arterial blood pressure. At the same dose, LV perfusion decreased by 23% (P=0.005) and CO decreased by 10% (P=0.003) owing to a decrease in heart rate (by 9%, P<0.002), with no significant changes in stroke volume or LV dimensions. Owing to the decreased CO and LV perfusion, systemic and coronary O2 delivery fell by 4 and 11% at 8 l of O2/min, despite the increased blood oxygen content.

CONCLUSION: Our data indicate that O2 administration decreases CO, LV perfusion and systemic and coronary O2 delivery in healthy individuals. Further research should address the effects of O2 therapy in normoxic patients.

Effects of oxygen inhalation on cardiac output, coronary blood flow and oxygen delivery in healthy individuals, assessed with MRI
European Journal of Emergency Medicine 2011, 18:25–30

RV involved in AMI more often than you think

We know that inferior STEMI may be complicated by right ventricular involvement, which is why I whack a V4R lead on all my inferior AMI patients. A recent study using cardiac magnetic resonance imaging showed that RV oedema and regional or global RV dysfunction were common in anterior infarcts too, although the proportion significantly decreased at four month follow up.

RV abnormalities are contiguous to the jeopardized LV myocardium and do not occur exclusively in inferior LV infarcts, but are found in up to 33% of anterior LV infarcts as well. The presence of RV ischemic injury is associated with early RV dysfunction as well as with RV functional recovery at follow-up.

Right Ventricular Ischemic Injury in Patients With Acute ST-Segment Elevation Myocardial Infarction: Characterization With Cardiovascular Magnetic Resonance.
Circulation. 2010 Oct 5;122(14):1405-12

‘AMI’ on ICU

ECG machines may give a printed report saying ***ACUTE MI***. In a retrospective study, patients on the ICU whose 12 lead ECGs contained this electronic interpretation did not have an elevated troponin 85% of the time. Even in the minority of patients whose electronic ECG diagnosis of MI was agreed with by a cardiologist, only one third developed an elevated troponin.

The authors state ‘In contrast to nonintensive care unit patients who present with chest pain, the electrocardiographic ST-segment elevation myocardial infarction diagnosis seems to be a nonspecific finding in the intensive care unit that is frequently the result of a variety of nonischaemic processes. The vast majority of such patients do not have frank ST-segment elevation myocardial infarction.’

Electrocardiographic ST-segment elevation myocardial infarction in critically ill patients: An observational cohort analysis
Crit Care Med. 2010 Dec;38(12):2304-230

Oxygen in AMI – no benefit, possible harm

A Cochrane review examined the evidence from randomised controlled trials to establish whether routine use of inhaled oxygen in acute myocardial infarction (AMI) improves patient-centred outcomes, the primary outcomes being death, pain and complications.

Three trials involving 387 patients were included and 14 deaths occurred. The pooled relative risk (RR) of death was 2.88 (95% CI 0.88 to 9.39) in an intention-to-treat analysis and 3.03 (95% CI 0.93 to 9.83) in patients with confirmed AMI. While suggestive of harm, the small number of deaths recorded meant that this could be a chance occurrence. Pain was measured by analgesic use. The pooled RR for the use of analgesics was 0.97 (95% CI 0.78 to 1.20).

There is therefore no conclusive evidence from randomised controlled trials to support the routine use of inhaled oxygen in patients with acute AMI. A definitive randomised controlled trial is required.

Oxygen therapy for acute myocardial infarction
Cochrane Review

Myocardial infarction not so common in LBBB?

An observational cohort study of 7937 ED visits by patients presenting with chest pain or ‘ischemic equivalent’ (shortness of breath for which ACS was considered a possible cause) was done to examine the relationship between left bundle branch block (LBBB) on the ECG and the incidence of acute myocardial infarction (AMI). No difference was observed in the rates of AMI in patients with new or presumed new LBBB, old LBBB, and no LBBB. The authors suggest that this large cohort of undifferentiated ED patients may be more reflective of the true prevalence of AMI in LBBB (7.3% in this study) and question the appropriateness of a liberal fibrinolytic strategy for such patients. Another argument for primary PCI?

Lack of association between left bundle-branch block and acute myocardial infarction in symptomatic ED patients
Am J Emerg Med. 2009 Oct;27(8):916-21

oxygen for myocardial infarction – harmful?

Hyperoxia may reduce coronary artery blood flow, increase systemic vascular resistance, and decrease cardiac output. This paper argues that if the baseline arterial oxygen saturations are >90%, high concentration oxygen does not increase oxygen transport, as the reductions in cardiac output are in excess of the increase in oxygen content. The balance of the limited evidence that exists suggests that the routine use of oxygen in uncomplicated MI (no failure or shock) may increase infarct size and possibly increase the risk of mortality, owing to its haemodynamic effects, including a reduction in coronary blood flow.

Routine use of oxygen in the treatment of myocardial infarction: systematic review
Heart. 2009 Mar;95(3):198-202